Cited by 411Atherosclerosis and Cardiovascular DiseasesPhagocytosis and Immune RegulationCholesterol and Lipid Metabolism

Mechanisms and consequences of macrophage apoptosis in atherosclerosis

Open access
Seimon, Tracie, Tabas, Ira·2009·Journal of Lipid Research

Abstract

Macrophage apoptosis is an important feature of atherosclerotic plaque development. Research directed at understanding the functional consequences of macrophage death in atherosclerosis has revealed opposing roles for apoptosis in atherosclerotic plaque progression. In early lesions, macrophage apoptosis limits lesion cellularity and suppresses plaque progression. In advanced lesions, macrophages apoptosis promotes the development of the necrotic core, a key factor in rendering plaques vulnerable to disruption and in acute lumenal thrombosis. The first section of this review will examine the role of phagocytic clearance of apoptotic macrophages, a process known as efferocytosis, in the dichotomous roles of macrophage apoptosis in early vs. advanced lesions. The second section will focus on the molecular and cellular mechanisms that are thought to govern macrophage death during atherosclerosis. Of particular interest is the complex and coordinated role that the endoplasmic reticulum (ER) stress pathway and pattern recognition receptors (PRRs) may play in triggering macrophage apoptosis.

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  • Apoptotic neutrophils are phagocytosed by macrophages, and macrophages can undergo apoptosis with clinical consequences such as atherosclerosis.

    “Apoptotic neutrophils are phagocytosed by macrophages [216], but macrophages also can undergo apoptosis, which may have important clinical consequences, such as atherosclerosis [217].”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [217]

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Research works printed but not linked: 14

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Authors
Seimon, T., & Tabas, I.
Affiliations
Columbia University (US)
Corresponding author
Tabas, Ira
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2009-04
Volume
50
Pages
S382-S387
ISSN
0022-2275 (ISSN-L)
OpenAlex
W2005861034
Cited by
411
References
1
Citations by year
2026: 8 · 2025: 15 · 2024: 20 · 2023: 14 · 2022: 24 · 2021: 28 · 2020: 26 · 2019: 29 · 2018: 18 · 2017: 27 · 2016: 38 · 2015: 20 · 2014: 26 · 2013: 31 · 2012: 26
FWCI
1.47
Type
journal article
Language
en
Open access
Locations
  • Journal of Lipid Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
National Heart, Lung, and Blood Institute (HL087123, P01HL054591, HL054591, HL075662, P01HL087123, R01HL075662)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
  • Life Sciences › Immunology and Microbiology › Immunology › Phagocytosis and Immune Regulation
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
Keywords
macrophage apoptosis, atherosclerosis, efferocytosis, phagocytosis of apoptotic cells, necrotic core, plaque vulnerability, endoplasmic reticulum stress, pattern recognition receptors, atherosclerotic plaque progression
MeSH terms
Animals, Endoplasmic Reticulum, Macrophages, Apoptosis, Atherosclerosis, Receptors, Pattern Recognition

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